Ascaris lumbricoides

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style="background:#Template:Taxobox colour;"|Ascaris lumbricoides
An adult female Ascaris worm
An adult female Ascaris worm
style="background:#Template:Taxobox colour;" | Scientific classification
Kingdom: Animalia
Phylum: Nematoda
Class: Secernentea
Order: Ascaridida
Family: Ascarididae
Genus: Ascaris
Species: A. lumbricoides
Binomial name
Ascaris lumbricoides
Linnaeus, 1758

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This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Ascariasis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]}}; Associate Editor-In-Chief: Imtiaz Ahmed Wani

Overview

Ascaris lumbricoides is the giant roundworm of humans, growing to a length of up to 35 cm (13.779527545 in).[1] It is one of several species of Ascaris. An ascarid nematode of the phylum Nematoda, it is the largest and most common parasitic worm in humans. This organism is responsible for the disease ascariasis, a type of helminthiasis and one of the group of neglected tropical diseases. An estimated one-sixth of the human population is infected by A. lumbricoides or another roundworm.[2] Ascariasis is prevalent worldwide, especially in tropical and subtropical countries.

Lifecycle

File:Ascaris lumbricoides life cycle.tif
Image showing lifecycle inside and outside of the human body of one fairly well described helminth: A. lumbricoides

A. lumbricoides, a roundworm, infects humans when an ingested fertilised egg becomes a larval worm that penetrates the wall of the duodenum and enters the blood stream. From there, it is carried to the liver and heart, and enters pulmonary circulation to break free in the alveoli, where it grows and molts. In three weeks, the larva passes from the respiratory system to be coughed up, swallowed, and thus returned to the small intestine, where it matures to an adult male or female worm. Fertilization can now occur and the female produces as many as 200,000 eggs per day for a year. These fertilized eggs become infectious after two weeks in soil; they can persist in soil for 10 years or more.[3]

The eggs have a lipid layer which makes them resistant to the effects of acids and alkalis, as well as other chemicals. This resilience helps to explain why this nematode is such a ubiquitous parasite.[4]

Morphology

File:Ascaris lumbricoides4.jpg
Fertile egg as can be seen in a microscope
File:Ascaris lumbricoides.jpg
Fertile egg in human faeces (detail)
File:Ascaris lumbricoides non-fertile egg.jpg
Infertile egg

A. lumbricoides is characterized by its great size. The male's posterior end is curved ventrally and has a bluntly pointed tail. Females are wide and long. The vulva is located in the anterior end and accounts for about one-third of its body length. Uteri may contain up to 27 million eggs at a time, with 200,000 being laid per day. Fertilized eggs are oval to round in shape and are long and wide with a thick outer shell. Unfertilized eggs measure long and wide.[5]

Genus and Species Ascaris lumbricoides
Common Name Giant Intestinal Roundworm
Etiologic Agent of: Ascariasis
Infective stage Embryonated Egg
Definitive Host Man
Portal of Entry Mouth
Mode of Transmission Ingestion of Embryonated egg through contaminated food or water
Habitat Small Intestine
Pathogenic Stage Adult Larva
Mode of Attachment Retention in the mucosal folds using pressure
Mode of Nutrition Feeding of Chyme
Pathogenesis Larva – pneumonitis, Loffler’s syndrome;

Goes through a Blood-Lung Phase (Hookworm and Strongyloides stercoralis also have a blood-lung phase); Adult worm– Obstruction, Liver abscess, Appendicitis.

Laboratory diagnosis Direct Fecal Smear; Concentration methods such as Kato-Katz
Treatment Albendazole, Mebendazole, or Pyrantel Pamoate
Diagnostic Feature - Adult Female - prominent genital girdle
Diagnostic Feature - Egg Coarse mammilated albuminous coating

Gallery

Epidemiology

More than 2 billion people are affected by this infection.[3] The United States has a reported prevalence of 0.8% of the total population as of 1987. A. lumbricoides eggs are extremely resistant to strong chemicals, desiccation, and low temperatures. The eggs can remain viable in the soil for several months or even years.[5]

Eggs of A. lumbricoides have been identified in archeological coprolites in the Americas, Europe, Africa, the Middle East, and New Zealand, the oldest ones being more than 24,000 years old.[7]

Infections

Infections with these parasites are more common where sanitation is poor,[8] and raw human feces are used as fertilizer.

Symptoms

Often, no symptoms are seen with an A. lumbricoides infection. However, in the case of a particularly bad infection, symptoms may include bloody sputum, cough, fever, abdominal discomfort, intestinal ulcer, passing worms, etc.[9][10] Ascariasis is also the most common cause of Löffler's syndrome worldwide. Accompanying symptoms include pulmonary infiltration, eosinophilia, and radiographic opacities [11]

Prevention

Preventing any fecal-borne disease requires educated hygienic habits/culture and effective fecal treatment systems. This is particularly important with A. lumbricoides because its eggs are one of the most difficult pathogens to kill (second only to prions), and the eggs commonly survive 1–3 years. A. lumbricoides lives in the intestine where it lays eggs. Infection occurs when the eggs, too small to be seen by the unaided eye, are eaten. The eggs may get onto vegetables when improperly processed human feces of infected people are used as fertilizer for food crops. Infection may occur when food is handled without removing or killing the eggs on the hands, clothes, hair, raw vegetables/fruit, or cooked food that is (re)infected by handlers, containers, etc. Bleach does not readily kill A. lumbricoides eggs, but it will remove their sticky film, to allow the eggs to be rinsed away. A. lumbricoides eggs can be reduced by hot composting methods, but to completely kill them may require rubbing alcohol, iodine, specialized chemicals, cooking heat, or "unusually" hot composting (for example, over 50 °C (122 °F) for 24 hours[12])

Details of infection process

Infections happen when a human swallows water or food contaminated with unhatched eggs, which hatch into juveniles in the duodenum. They then penetrate the mucosa and submucosa and enter venules or lymphatics. Next, they pass through the right heart and into pulmonary circulation. They then break out of the capillaries and enter the air spaces. Acute tissue reaction occurs when several worms get lost during this migration and accumulate in other organs of the body. The juveniles migrate from the lung up the respiratory tract to the pharynx where they are swallowed. They begin producing eggs within 60–65 days of being swallowed. These are produced within the small intestine, where the juveniles mature. It might seem odd that the worms end up in the same place where they began. One hypothesis to account for this behavior is that the migration mimics an intermediate host, which would be required for juveniles of an ancestral form to develop to the third stage. Another possibility is that tissue migration enables faster growth and larger size, which increases reproductive capacity.[13]

Diagnosis and treatment

Most diagnoses are made by identifying the appearance of the worm or eggs in feces. Due to the large quantity of eggs laid, physicians can diagnose using only one or two fecal smears.[citation needed]

Infections can be treated with drugs called ascaricides. The treatment of choice is mebendazole. The drug functions by binding to tubulin in the worms' intestinal cells and body-wall muscles. Nitazoxanide and ivermectin can also be used.[5]

References

  1. "eMedicine - Ascaris Lumbricoides : Article by Aaron Laskey". Archived from the original on 27 January 2008. Retrieved 2008-02-03.
  2. Harhay, Michael O; Horton, John; Olliaro, Piero L (2010). "Epidemiology and control of human gastrointestinal parasites in children". Expert Review of Anti-infective Therapy. 8 (2): 219–34. doi:10.1586/eri.09.119. PMC 2851163. PMID 20109051.
  3. 3.0 3.1 Murray, Patrick R.; Rosenthal, Ken S.; Pfaller, Michael A. Medical Microbiology, Fifth Edition. United States: Elsevier Mosby, 2005Template:Pn
  4. Piper R (2007). Extraordinary Animals: An Encyclopedia of Curious and Unusual Animals, Greenwood Press.Template:Pn
  5. 5.0 5.1 5.2 Roberts, Larry S.; Janovy, John Jr. Foundations of Parasitology, Eighth Edition. United States: McGraw-Hill, 2009Template:Pn
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 "Public Health Image Library (PHIL)".
  7. Dridelle R. Parasites. Tales of Humanity's Mostly Unwelcome Guests. Univ. of California, 2010. p. 26. ISBN 978-0-520-25938-6.
  8. "DPDx - Ascariasis". Archived from the original on 24 February 2008. Retrieved 2008-02-03.
  9. MedlinePlus Encyclopedia Ascariasis
  10. http://www.stanford.edu/group/parasites/ParaSites2005/Ascaris/JLora_ParaSite.htm#Symptoms[full citation needed]
  11. Löffler, W (1956). "Transient Lung Infiltrations with Blood Eosinophilia". International Archives of Allergy and Applied Immunology. 8 (1–2): 54–9. doi:10.1159/000228268. PMID 13331628.
  12. http://weblife.org/humanure/chapter7_18.html[full citation needed]
  13. Read, A. F.; Sharping, A. (1995). "The evolution of tissue migration by parasitic nematode larvae". Parasitology. 111 (3): 359–71. doi:10.1017/S0031182000081919. PMID 7567104.

External links

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